Cilia are important motile cell organelles of organisms including man. This study continues a comprehensive attack on the structure and function of cilia, particularly centering on ultrastructural correlates of ciliary motion, and cellular control of motility. It is likely that the mechanism of motility, common to all motile somatic cell cilia, involves microtubule sliding. Several major events in the sliding microtubule model have been established previously, but this work seeks to extend the model (1) By direct visualization of a postulated radial spoke cycle that is thought to convert sliding into local bending during the ciliary stroke, (2) By determining the direction of active sliding, and (3) By examining the controls necessary to arrest cilia (by inhibiting co-ordinated sliding?). Behavioral controls such as ciliary arrest all seem to depend upon the common mechanism of increase in Ca ions concentration in the cell cytoplasm, or in the axoneme. This work seeks to demonstrate whether Ca ions influx is related to the spreading arrest and recovery induced by local laser lesions in certain ciliated epithelia and whether Ca ions controls sliding by direct interaction with components of the axoneme including the dynein arms and the spokes. The entry of Ca ions is via the cell membrane; in particular, particle arrays such as the ciliary necklace and patches at the base of the ciliary membrane are possible parts of the permeability pathway. This work seeks to characterize such arrays in freeze fracture and examine aspects of their biochemistry, morphogenesis and assembly, as well as their relationship to Ca ions control of sliding. Knowledge such as this may enable us to understand or prevent ciliary malfunction that can, for example, precipitate respiratory disease.